From over to underactive bladder - mechanisims biomarkers and treatments

Round Table Discussion 3

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START END TOPIC SPEAKER
11:00 11:10 Overview Roger Dmochowski
11:10 11:30 Impact of fibrosis and treatments Anthony Kanai
11:30 11:50 Neuromodulation in treatment of UAB Gommert van Koeveringe
11:50 12:00 Take home message Laurence Stewart

Roger Dmochowski
A variety of putative mechanistic explanations have been advanced as to the etiologic causation and contributions to underactive bladder (UAB) as a condition. Comorbidities heretofore advanced include: aging related changes (either myopathic or neuropathic in nature), unrecognized myopathic or neuropathic disease unrelated to age, vascular based phenomena (ischemia and reperfusion), and obstructive conditions. Evidence supporting these contributing etiologies will be reviewed and an effort will be made to provide a composite summary of current knowledge of the pathophysiology of UAB. Potential implications for therapeutic intervention will also be discussed.

Anthony Kanai
This round table will discuss mechanisms, biomarkers and treatments for underactive bladder (UAB) with my talk focusing on bladder fibrosis and its treatment. It’s noteworthy that about 45% of all deaths in the developed world are attributable to fibroproliferative diseases of muscle of various organ systems. In the lower urinary tract, urethral and prostatic fibrosis can contribute to outlet obstruction, while chronic cystitis due to ketamine abuse or radiation therapy may result in acontractile bladders. Anti-inflammatory agents can limit collagen deposition, while the new anti-fibrotic agent human relaxin-2 reverses fibrosis by degrading excess collagen and stopping its further deposition.

Gommert A. van Koeveringe
In case of an underactive bladder the evacuating function of the bladder is dysfunctional due to a disbalance of detrusor contractile capacity and the subvesical relaxation capacity. Both of these functions are regulated by supraspinal, spinal and possibly also local reflexes. A decay of bladder and urethral afferent function or perception of these signals by our higher brain centers has been shown to play a major role in the etiology of UAB. A tool to regain control over the reflexes involved is sacral neuromodulation. Therefore, dependent on the condition responsible for the underactive bladder, neuromodulation is expected to play a crucial role in the treatment of UAB.